Smart Energy Clays: Chemical Vapor Deposition of PEDOT in Expanded Vermiculite Blocks for Electrochemical Energy Storage

With rapid development of sustainable energy storage systems and intelligent energy supply equipment, supercapacitors have attracted wide attention while still suffering from low specific capacitance, poor kinetic diffusion, and charge transfer. Here, we demonstrate the concept of integrating conductive polymer poly(3,4-ethylenedioxythiophene) (PEDOT) into insulation voids in expanded vermiculite blocks, achieving PEDOT-intercalated vermiculite electrodes for pseudocapacitive energy storage. The electrodes show rapid kinetic diffusion and charge transfer as well as high areal specific capacitance of 2592 mF cm–2 at the current density of 3 mA cm–2, surpassing most of the state-of-the-art electrodes for supercapacitors. The prepared electrodes were assembled into a symmetrical supercapacitor which shows a specific capacitance of 412.8 mF cm–2 at a current density of 2 mA cm–2 with a high energy density of 30.3 μW h cm–2 at a high power density of 3001.8 μW cm–2. This work realizes the preparation of electrochemical energy storage electrode materials on insulating layer minerals, which is a fruitful tactic and opens the door to the creation of more supercapacitor electrodes

Image_1_Giant functional parathyroid carcinoma: a case report and literature review.jpeg

BackgroundParathyroid carcinoma is an infrequent neoplasm of the endocrine system, constituting roughly 0.5% to 5% of cases of primary hyperparathyroidism. The diagnosis of this condition presents a unique challenge for healthcare professionals.Case reportWe present a case of a 77-year-old female patient who presented with a longstanding right-sided neck tumor. The Positron emission tomography-computed tomography (PET-CT) scan detected a substantial tumor situated at the inferior border of the thyroid gland. A surgical procedure was conducted, resulting in the total excision of the tumor. The diagnosis of parathyroid carcinoma was confirmed through pathological investigation. At the six-month follow-up, the patient exhibited favorable post-operative outcomes with no evidence of recurrence.ConclusionThe primary approaches for managing parathyroid carcinoma involve precise diagnosis and surgical removal. This case report provides confirmation that the implementation of rigorous treatment measures can yield a substantial improvement in the prognosis.</p

Sequences of Primers Used for Quantitative Real-time PCR.

Sequences of Primers Used for Quantitative Real-time PCR.</p

Icariin increases chondrocytes proliferation.

<p>(A) MTT assay for cell viability of chondrocytes treated with or without Icariin (0 M, 10⁻⁷ M, 10⁻⁶ M, 10⁻⁵ M) for 3 days. Treated groups compared with control group, *<i>P</i> < 0.05, **<i>P</i> < 0.01, n = 3. (B) BrdU incorporation assay for chondrocytes treated with or without Icariin (0 M, 10⁻⁷ M, 10⁻⁶ M, 10⁻⁵ M) for 1 day or 3 days. Treated groups compared with control group, *<i>P</i> < 0.05; ***<i>P</i> < 0.001, n = 3. (C) Colony formation assay for chondroprogenitor cells treated with Icariin (10⁻⁷ M, 10⁻⁶ M, 10⁻⁵ M) for 24 h followed by 14 days sub-culture. (D) Quantitation of the colony numbers from (C), *<i>P</i> < 0.05, n = 3.</p

Icariin promotes articular cartilage repair in the mouse osteochondral defect model.

3D complexes incorporated with or without Icariin were transplanted in osteochondral defect regions of the distal femur of mice (detailed in Material and Methods). The dashed lines surround the newly formed tissue in the osteochondral defect region. (A) H&E staining showed the osteochondral defect regions in Icariin treated group and control group at 2 weeks post-transplantation. Scale bar = 200 μm. (B) Immunostaining for PCNA in the sections from icariin treated group and control group at 2 weeks post-transplantation. Upper panel, low magnification, Scale bar = 200 μm. Lower panel, high magnification, Scale bar = 50 μm. (C) Quantitation of the percentage of PCNA+ cells in the PCNA-stained sections represented in (B). *P P P P < 0.05, n = 5.</p

Icariin enhances chondrogenic marker expression and cartilage matrix synthesis while the effect is limited by knockdown of HIF-1α.

<p>(A) Chondrocytes were processed for micromass culture and induced to differentiate in chondrogenic medium in the presence or absence of Icariin (10⁻⁷ M, 10⁻⁶ M, 10⁻⁵ M). The cell masses were stained with Alcian blue after 7 or 14 days culture, respectively. Note that Icariin (10⁻⁶ M) increased proteoglycan synthesis. (B) Quantitation of the value of integral optical density (IOD) from (A). Treated groups compared with control group, *<i>P</i> < 0.05; **<i>P</i> < 0.01; ***<i>P</i> < 0.01, n = 3. (C, D) ELISA assays for production of aggrecan (C) and hydroxypoline (D) in chondrocytes. Icariin treated groups versus control groups, *<i>P</i> < 0.05; **<i>P</i> < 0.01; ***<i>P</i> < 0.001, n = 3. (E, F) Chondrocytes were cultured and induced to differentiate in chondrogenic medium in the presence or absence of Icariin (10⁻⁶ M) for 7 (E) or 14 (F) days. <i>Sox9</i>, <i>Col2α1</i> and <i>Aggrecan</i> mRNA expression was detected by real-time PCR in Icariin treated chondrocytes and compared with that in the control cells. *<i>P</i> < 0.05, **<i>P</i> < 0.01; ***<i>P</i> < 0.001, n = 3.</p

Icariin increases chondrocyte proliferation accompanied by upregulation of HIF-1α in alginate-chondrocyte 3D culture system.

<p>(A) Representative images of immunostaining for PCNA in 3D cultured sections from Icariin treated group and control group. Arrows indicate PCNA⁺ chondrocytes. IgG was used as negative control. Scale bar = 50 μm. (B) Quantitation of the percentage of PCNA positive cells in the Icariin treated group and control group. *<i>P</i> < 0.05, n = 3. (C) Representative images of immunostaining for HIF-1α in 3D cultured sections from Icariin treated group and control group. Arrows indicate HIF-1α positive (HIF-1α+) chondrocytes. IgG was used as negative control. Scale bar = 50 μm. (D) Quantitation of the percentage of HIF-1α+ cells in the sections from Icariin treated groups and control groups. *<i>P</i> < 0.05, n = 3.</p

Icariin upregulates HIF-1α expression in chondrocytes by inhibiting PHDs activity through competition for iron ions.

<p>(A) The chemical formula of Icariin. (B) Hypoxia response element luciferase reporter assay in C2C12 cells treated with Icariin at indicated concentrations. (C) Western blot analysis for HIF-1α protein expression in primary culture-derived chondrocytes under normoxia or hypoxia or treated with or without Icariin (10⁻⁶ M) for 8 h. β-actin used as the loading control. (D) Detection of HIF-1α nuclear localization in Icariin (10⁻⁶ M)-treated chondrocytes by immunofluorescence staining under confocal microscope. (E, F) Chondrocytes were cultured and induced to differentiate in chondrogenic medium in the presence or absence of Icariin (10⁻⁶ M) for 7 or 14 days. HIF-1α mRNA levels were detected by real-time PCR in Icariin-treated chondrocytes compared with that of the control cells. *<i>P</i> < 0.05, **<i>P</i> < 0.01, n = 3. (G) UV-Vis spectra of the Icariin, FeSO₄ and their mixture (<i>n</i>_Icariin: <i>n</i>_FeSO4 = 3: 1, <i>C</i>_Icariin = 0.5mM) in aqueous solution after incubation at 37°C for 12 h; <i>C</i>_Icariin = 0.5mM; <i>C</i>_FeSO4 = 1mM; The inset shows the visual appearance of each species. (H) Western blot analysis for HIF-1α protein expression in chondrocytes treated with or without Icariin (10⁻⁶ M) and FeSO₄ (100 μM) for 12 h. (I) Western blot analysis for PHDs and HIF-1α protein expression in chondrocytes treated with or without Icariin (10⁻⁶ M) for 12 h. In all Figs, ICA, Icariin.</p

Deletion of HIF-1α eliminates the positive effects of Icariin on chondrocytes.

<p>(A) Western blot analysis for HIF-1α protein expression in MSCs (HIF-1α Floxed) following treatment with Ad-GFP or Ad-Cre and treated with or without Icariin (10⁻⁶ M) for 12 h. β-actin used as the loading control. (B) Alcian blue staining for preoteoglycan synthesis in MSCs (HIF-1α floxed) following treatment with Ad-GFP or Ad-Cre and treated with or without Icariin (10⁻⁶ M) for 14 days. (C) Quantitation of the value of integral optical density (IOD) from (B). Compared with Ad-GFP-treated control group, *<i>P</i> < 0.05; n = 3. (D) BrdU incorporation assay for chondrocytes following treatment with Ad-GFP or Ad-Cre and treated with or without Icariin (10⁻⁶ M) for 48 h. Compared with Ad-GFP-treated control group, *<i>P</i> < 0.05, **<i>P</i> < 0.01; n = 3. Compared with Ad-GFP-treated ICA control group, ^##<i>P</i> < 0.01; n = 3. (E, F) Chondrocytes following treatment with Ad-GFP or Ad-Cre were cultured under normal medium in the presence or absence of Icariin (10⁻⁶ M). (E) <i>Sox9</i>, <i>Aggrecan</i> and <i>Col2α1</i> mRNA expression in chondrocytes was detected by real-time PCR. (F) <i>Adamts4</i>, <i>Mmp2</i>, and <i>Mmp9</i> mRNA expression in chondrocytes was detected by real-time PCR. Compared with Ad-GFP-treated control group,*<i>P</i> < 0.05, **<i>P</i> < 0.01; n = 3. Compared with Ad-Cre-treated control group, ^#<i>P</i> < 0.05; ^##<i>P</i> < 0.01; n = 3.</p

Icariin inhibits catabolic marker genes expression in chondrocytes.

<p>Chondrocytes were cultured and induced to differentiate in chondrogenic medium in the presence or absence of Icariin (10⁻⁶ M) for 7 (A) or 14 (B) days. <i>Mmp2</i>, <i>Mmp9</i>, <i>Mmp13</i>, <i>Adamts4</i> and <i>Adamts5</i> mRNA expression was detected by real-time PCR in Icariin treated chondrocytes compared with that of the control cells. *<i>P</i> < 0.05; **<i>P</i> < 0.01; n = 3.</p